Endothelial and vascular smooth muscle responses are altered after left lung autotransplantation

1994 ◽  
Vol 266 (5) ◽  
pp. H2026-H2032 ◽  
Author(s):  
N. A. Flavahan ◽  
T. D. Aleskowitch ◽  
P. A. Murray
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Left Lung ◽  
Calcium Ionophore ◽  
Selective Reduction ◽  
Isometric Tension ◽  
Maximal Response ◽  
No Donor ◽  
Significant Difference ◽  
Increased Sensitivity

Left lung autotransplantation (LLA) increased the pulmonary vasoconstriction evoked by phenylephrine and attenuated the vasodilatation caused by acetylcholine or bradykinin in conscious dogs. To study the mechanisms responsible for these changes, pulmonary arterial rings were isolated from right (control) and left (LLA) lower lobes of dogs 1-26 mo after LLA and were suspended for isometric tension recording. Compared with control rings from the same anatomic location, contractions to phenylephrine were increased after LLA in rings with or without endothelium. In arterial rings contracted to 50% of their maximal response to phenylephrine, acetylcholine, bradykinin, and calcium ionophore caused endothelium-dependent relaxations that were reduced in LLA compared with control rings. In arterial rings from control and LLA lungs, relaxations to acetylcholine were not altered by inhibition of cyclooxygenase (indomethacin) but were reduced after inhibition of NO synthase [N omega-nitro-L-arginine methyl ester (L-NAME)]. After L-NAME, there was no longer any significant difference in acetylcholine-induced relaxation between arterial rings from control and LLA lungs. Relaxation to SIN-1, a NO donor, was similar in arterial rings (without endothelium) from control and LLA lungs. The results suggest that LLA causes an increased sensitivity of vascular smooth muscle to alpha 1-adrenergic activation and endothelial dysfunction that is mediated by a selective reduction in the activity of endothelium-derived relaxing factor/NO.

Stimulus-response relationships for isotonic shortening and isometric tension generation in rabbit trachealis

1994 ◽  
Vol 77 (4) ◽  
pp. 1638-1643 ◽  
Author(s):  
A. Opazo-Saez ◽  
P. D. Pare
Keyword(s):  
Smooth Muscle ◽  
Isometric Force ◽  
Electrical Field Stimulation ◽  
Isometric Tension ◽  
Maximal Response ◽  
Field Stimulation ◽  
Electrical Field ◽  
Increased Sensitivity ◽  
Isotonic Shortening

Nonspecific bronchial hyperresponsiveness in asthma is characterized by increased maximal airway narrowing (reactivity) and increased sensitivity of the airways. A decreased load on airway smooth muscle (ASM) has been suggested as a mechanism of increased reactivity. We hypothesized that decreased ASM load can also cause a leftward shift in the dose-response curve and explain increased sensitivity. We tested this hypothesis using rabbit tracheal smooth muscle strips in vitro by measuring isotonic shortening and isometric force during electrical field stimulation (1–100 Hz) at the length at which maximal active tension developed (Lmax), 90% Lmax, and 110% Lmax The frequency-response relationships expressed as frequency vs. percent maximal shortening or tension were not different at Lmax or 110% Lmax, but at 90% Lmax the frequency vs. shortening relationship was significantly shifted leftward relative to the frequency vs. tension relationship (P < 0.05). The electrical field stimulation frequencies that produced 50% maximal response for isometric tension and for isotonic shortening, respectively, were 6.7 +/- 1.9 and 3.9 +/- 0.7 Hz at 90% Lmax, 9.2 +/- 2.1 and 7.5 +/- 1.9 Hz at 100% Lmax, and 2.8 +/- 1.0 and 1.2 +/- 0.5 Hz at 110% Lmax. We conclude that, at lengths below Lmax, isotonic shortening is facilitated compared with isometric tension and therefore decreased ASM load in vivo may result in increased sensitivity.

Vascular smooth muscle responsiveness in a hibernator: effects of season and temperature

1986 ◽  
Vol 250 (1) ◽  
pp. R77-R82 ◽  
Author(s):  
V. M. Miller ◽  
W. L. Miller ◽  
F. E. South
Keyword(s):  
Smooth Muscle ◽  
Portal Vein ◽  
Vascular Smooth Muscle ◽  
Bath Temperature ◽  
Isometric Tension ◽  
Physiological Salt Solution ◽  
Organ Bath ◽  
Response Curves ◽  
Renal Vessels ◽  
Increased Sensitivity

To determine the effects of season, acclimation state, and hibernation on the reactivity of vascular smooth muscle from a hibernant species, strips of thoracic aorta, renal and femoral arteries, and portal vein obtained from adult woodchucks, Marmota monax, were suspended for isometric tension measurements in physiological salt solution. These blood vessels exhibited no seasonal variation in resting tension, connective tissue content, or maximum tension developed to norepinephrine. However, the concentration-response curves to norepinephrine in both aortic and portal vein strips from animals tested in May and June were shifted to the left of those from animals tested in either August or November through February. This increased sensitivity to the catecholamine was seen also in renal vessels from hibernating compared with nonhibernating animals. Decreasing organ bath temperature from 37 to 28 degrees C increased tension developed in response to norepinephrine in aortic and renal strips, whereas that of the femoral artery was unchanged. With further cooling to 17 degrees C, the responses to norepinephrine in aortic and renal strips were similar to the responses at 37 degrees C. The contraction developed to 40 mM KCl was diminished in all tissues at 28 degrees C. Blockade of beta-adrenergic receptors did not augment the response to norepinephrine at 37 degrees C. Contractions of the woodchuck aorta in calcium-free medium were sustained longer than comparable tissue obtained from a rabbit. These data suggest that receptor-mediated processes are modulated in hibernating animals. This modulation varies among vascular beds and may act to maintain or divert perfusion of the tissue through entry, during, and arousal from hibernation.

Short-term exercise training alters responses of porcine femoral and brachial arteries

1997 ◽  
Vol 82 (5) ◽  
pp. 1438-1444 ◽  
Author(s):  
Richard M. McAllister ◽  
M. Harold Laughlin
Keyword(s):  
Exercise Training ◽  
Citrate Synthase ◽  
Calcium Ionophore ◽  
Maximal Response ◽  
Short Term ◽  
Miniature Swine ◽  
Vascular Rings ◽  
Increased Sensitivity ◽  
Relaxation Responses

McAllister, Richard M., and M. Harold Laughlin.Short-term exercise training alters responses of porcine femoral and brachial arteries. J. Appl. Physiol. 82(5): 1438–1444, 1997.—The primary purpose of this study was to test the hypothesis that short-term exercise training enhances endothelium-dependent relaxation of porcine femoral and brachial arteries. Miniature swine ran on a treadmill for 1 h at 3.5 miles/h, twice daily, for 7 consecutive days (Trn; n = 8). Compared with sedentary controls (Sed; n = 7), Trn swine exhibited increased skeletal muscle citrate synthase activity ( P < 0.05). Vascular rings ∼3 mm in axial length were prepared from segments of femoral and brachial arteries, and responses to vasoactive agents were determined in vitro. Sensitivity to bradykinin (BK) was enhanced in brachial vascular rings from Trn swine compared with those from Sed swine, as indicated by lower concentration of vasorelaxing agent eliciting 50% of maximal response values [Sed, 8.63 ± 0.09 (−log M); Trn, 9.07 ± 0.13; P < 0.05]. This difference between groups was preserved in brachial rings in which formation of nitric oxide and vasodilator prostaglandins were inhibited [Sed, 8.57 ± 0.17 (−log M); Trn, 8.97 ± 0.13; P < 0.05]. Sensitivity to BK was not different between Sed and Trn in femoral arterial rings. Relaxation responses to the calcium ionophore A-23187 and sodium nitroprusside were not altered with training. Femoral and brachial arterial rings from Trn swine, compared with those from Sed swine, exhibited augmented vasocontraction across a range of concentrations and increased sensitivity to norepinephrine (all P < 0.05). These findings indicate that responses of porcine femoral and brachial arteries change in response to short-term training. Together with findings from previous studies involving longer term training, our data suggest that vascular adaptations may differ at different time points during long-term endurance exercise training.

Effect of SR-49059, a vasopressin V1a antagonist, on human vascular smooth muscle cells

1995 ◽  
Vol 268 (1) ◽  
pp. H404-H410 ◽  
Author(s):  
C. Serradeil-Le Gal ◽  
J. M. Herbert ◽  
C. Delisee ◽  
P. Schaeffer ◽  
D. Raufaste ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Specific Binding ◽  
Muscle Cells ◽  
Maximal Response ◽  
Receptor Subtypes ◽  
Functional Studies ◽  
Antagonist Binding

The effects of SR-49059, a new nonpeptide and selective arginine vasopressin (AVP) V1a antagonist, were investigated in binding and functional studies on cultured human aortic vascular smooth muscle cells (VSMC). Characterization of human vascular V1a receptors, using a specific V1a radioiodinated ligand, showed that [125I]-linear AVP antagonist binding to human VSMC membranes was time dependent, reversible, and saturable. A single population of high-affinity binding sites (apparent equilibrium dissociation constant = 15 +/- 6 pM; maximum binding density = 36 +/- 5 fmol/mg protein, i.e., approximately 3,000 sites/cell) with the expected V1a profile was identified. Exposure of these cells to AVP dose-dependently produced cytosolic free [Ca2+] increase [AVP concentration required to obtain a half-maximal response (EC50) = 23 +/- 9 nM] and proliferation (EC50 = 3.2 +/- 0.5 nM). SR-49059 strongly and stereospecifically inhibited [125I]-linear AVP antagonist binding to VSMC V1a receptors [inhibition constant (Ki) = 1.4 +/- 0.3 nM], AVP-evoked Ca2+ increase [concentration of inhibitor required to obtain 50% inhibition of specific binding (IC50) = 0.41 +/- 0.06 nM], and the mitogenic effects induced by 100 nM AVP (IC50 = 0.83 +/- 0.04 nM). OPC-21268, another nonpeptide V1a antagonist, was more than two orders of magnitude less potent than SR-49059 in these models. However, the consistent affinity (Ki = 138 +/- 21 nM) and activity found with OPC-21268 on human VSMC in comparison with the inactivity already observed for other human V1a receptors (liver, platelets, adrenals, and uterus) strongly suggested the existence of human AVP V1a-receptor subtypes.(ABSTRACT TRUNCATED AT 250 WORDS)

Binding, degradation, and biological activity of insulin in vascular smooth muscle cells

1985 ◽  
Vol 249 (3) ◽  
pp. E292-E298
Author(s):  
N. Kaiser ◽  
A. Tur-Sinai ◽  
M. Hasin ◽  
E. Cerasi
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cultured Cells ◽  
Muscle Cells ◽  
Insulin Binding ◽  
Maximal Response ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Igf I

The interaction of insulin with the vascular smooth muscle was studied using cultures derived from the bovine aortic arch. The cultured cells exhibited specific binding of 125I-insulin that was reversible and dependent on pH. Both insulin and insulinlike growth factor (IGF) I competed for 125I-insulin binding; IGF I, however, was less effective than insulin by at least an order of magnitude. Insulin binding was accompanied by internalization and degradation of the hormone in a temperature- and time-dependent manner. Chloroquine and other lysosomotropic agents elevated the internalized insulin and reduced its degradation. Pre-exposure of cell cultures to insulin resulted in downregulation of cell surface receptors. Insulin stimulated alpha-aminoisobutyric acid transport in confluent smooth muscle cells. The maximal response was observed at 100 ng/ml insulin with a half-maximal effect at 10 ng/ml. Sparse, serum-starved smooth muscle cells responded to insulin with a dose-dependent increase in [3H]-thymidine incorporation into DNA. Although the effect was already apparent at 1 ng/ml insulin, it reached near maximal level only at 10,000 ng/ml. IGF I also stimulated DNA synthesis in smooth muscle cells; however, at low concentrations insulin was more efficient in this respect. Human growth hormone was inactive. The data indicate the presence of specific receptors for insulin in bovine aortic smooth muscle cells. These receptors appear to mediate the metabolic activity as well as part of the mitogenic effect of insulin in these cells.

Heterogeneous distribution of endothelium-dependent relaxations resistant to NG-nitro-L-arginine in rats

1992 ◽  
Vol 263 (4) ◽  
pp. H1090-H1094 ◽  
Author(s):  
T. Nagao ◽  
S. Illiano ◽  
P. M. Vanhoutte
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Calcium Ionophore ◽  
Renal Arteries ◽  
Mesenteric Arteries ◽  
K Channel ◽  
Ionophore A23187 ◽  
Dependent Manner ◽  
Arterial Tree ◽  
Heterogeneous Distribution

Endothelium-dependent relaxations that are resistant to inhibitors of nitric oxide synthase probably are mediated by endothelium-dependent hyperpolarization of the vascular smooth muscle. Experiments were performed to examine the distribution of this type of relaxation along the arterial tree of the rat by measuring changes in isometric force. Acetylcholine induced concentration- and endothelium-dependent relaxations in aortas and in pulmonary, common iliac, femoral, mesenteric, and renal arteries contracted with phenylephrine. In the presence of NG-nitro-L-arginine, the cumulative administration of acetylcholine induced relaxations only in the femoral, mesenteric, and renal arteries. The calcium ionophore A23187 relaxed mesenteric arteries contracted with phenylephrine in a concentration- and endothelium-dependent manner. The concentration-relaxation curve to A23187 was shifted to the right in the presence of NG-nitro-L-arginine. The maximal relaxations induced by lemakalim, a K+ channel opener, were smaller in those arteries that did not exhibit NG-nitro-L-arginine-resistant relaxations. These results suggest that NG-nitro-L-arginine-resistant relaxations are more frequently observed in smaller arteries. The arteries that exhibit NG-nitro-L-arginine-resistant relaxations may be more sensitive to an endothelium-derived substance that causes hyperpolarization of vascular smooth muscle cells.

Does heparin inhibit renin activity?

1991 ◽  
Vol 69 (9) ◽  
pp. 1360-1363 ◽  
Author(s):  
Masato Matsunaga ◽  
Yoko Yamanaka ◽  
Noriko Nagano ◽  
Yuki Iwasaki ◽  
Yumi Saito ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Substrate ◽  
Significant Difference ◽  
Inactive Renin

Although heparin was reported in the 1960s to inhibit renin activity, this has not always been confirmed by other investigators. Hence, we re-examined whether heparin really inhibits renin or not. Renin activities were determined by radioimmunoassay of angiotensin I generated at pH 7.4. (i) No significant difference was found between the two kinds of plasma samples obtained with heparin and with EDTA as anticoagulant, in ARC (renin activity with addition of sheep renin substrate), TRC (ARC after activation of inactive renin by trypsin), or PRA (plasma renin activity without additional substrate), (ii) Even in higher concentrations of heparin up to 500 U/mL, neither PRA, ARC, nor TRC of plasma was affected significantly. (iii) Heparin, in concentrations up to 500 U/mL, exerted no significant effect on TRC of the media of human vascular smooth muscle cell culture. In conclusion, heparin does not exert any significant inhibitory effect on human renin nor does it affect activation of inactive renin by trypsin in the range of concentration of practical use, under the conditions employed in this study.Key words: plasma renin, tissue renin, inactive renin, vascular smooth muscle cell, trypsin.

Melatonin potentiates contractile responses to serotonin in isolated porcine coronary arteries

2001 ◽  
Vol 280 (1) ◽  
pp. H76-H82 ◽  
Author(s):  
Qiong Yang ◽  
Elizabeth Scalbert ◽  
Philippe Delagrange ◽  
Paul M. Vanhoutte ◽  
Stephen T. O'Rourke
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Smooth Muscle ◽  
Coronary Arteries ◽  
Isometric Tension ◽  
Maximal Response ◽  
Melatonin Receptor ◽  
Vasomotor Tone ◽  
Vasoconstrictor Response ◽  
Coronary Vasomotor Tone

The present study was designed to determine the effects of melatonin on coronary vasomotor tone. Porcine coronary arteries were suspended in organ chambers for isometric tension recording. Melatonin (10−10-10−5 M) itself caused neither contraction nor relaxation of the tissues. Serotonin (10−9-10−5 M) caused concentration-dependent contractions of coronary arteries, and in the presence of melatonin (10−7 M) the maximal response to serotonin was increased in rings with but not without endothelium. In contrast, melatonin had no effect on contractions produced by the thromboxane A2 analog U-46619 (10−10-10−7 M). The melatonin-receptor antagonist S-20928 (10−6 M) abolished the potentiating effect of melatonin on serotonin-induced contractions in endothelium-intact coronary arteries, as did treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10−5 M), methylene blue (10−5 M), or NG -nitro-l-arginine (3 × 10−5 M). In tissues contracted with U-46619, serotonin caused endothelium-dependent relaxations that were inhibited by melatonin (10−7 M). Melatonin also inhibited coronary artery relaxation induced by sodium nitroprusside (10−9-10−5 M) but not by isoproterenol (10−9-10−5 M). These results support the hypothesis that melatonin, by inhibiting the action of nitric oxide on coronary vascular smooth muscle, selectively potentiates the vasoconstrictor response to serotonin in coronary arteries with endothelium.

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